New Treatment Target for Acute Myeloid Leukemia


Inhibiting GCN5 enzyme may lead to reduced remission risks and improved cure rates.

New insight in the fight against acute myeloid leukemia (AML) may provide new opportunities for more effective treatment.

AML is caused by an overproduction of impaired white blood cells. A key process for mediating the body’s immunity is the differentiation of immature white blood cell precursors into functional white blood cells.

A study published in Nature Communications revealed the discovery of the enzyme GCN5, which can inactivate the protein C/EBPa in myeloid precursor cells. This inactivity results in immature myeloid white blood cells being unable to mature into granulocytes and results in disrupting the formation of healthy white blood cells.

Acetylation has been found to carry out the inactivation of C/EBPa as GCN5 adds an acetyl group onto C/EBPa, reducing the protein’s ability to bind to DNA and modulating its transcriptional activity in the cell.

“As AML is a fast-growing cancer, timely treatment soon after diagnosis could increase patients' chances of survival,” said Daniel Tenen, Director of CSI Singapore. “The current main treatment strategy for AML is cytotoxic chemotherapy. Our research results form the basis of an alternative therapeutic strategy that could potentially reduce remission risks and improve cure rates. Moving forward, the team is looking into designing effective GCN5 inhibitors for therapeutic purposes by studying GCN5 in AML further in depth.”

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